PANK2 and neoplasm: Although ACLY inhibition has been shown to suppress tumour proliferation in many preclinical models18–20, its therapeutic potential has been questioned due to compensatory upregulation of alternative acetyl-CoA-generating pathways, including acetate CoA synthetase 2 (ACCS2)8,10, pyruvate dehydrogenase (PDH)9,10, pantothenate kinase 2 (PANK2)11 and fatty acid oxidation12, that may bypass ACLY dependency.